Linked Life Data

3508430

Source:http://linkedlifedata.com/resource/pubmed/id/3508430

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-5
pubmed:dateCreated
1989-6-12
pubmed:abstractText
Perfusion of isolated rat livers with ethanol at a concentration of 2 g/l (%o) resulted in a release of glutamate-pyruvate-transaminase (GPT) and sorbitol dehydrogenase (SDH) into the perfusate as markers of toxicity. Inhibition of alcohol dehydrogenase by 4-methylpyrazole or of aldehyde dehydrogenase by cyanamide totally abolished ethanol hepatotoxicity despite of a severalfold increase in acetaldehyde concentration in the perfusate. Addition of superoxide dismutase or catalase clearly suppressed the ethanol-induced release of GPT and SDH, suggesting that .O2- and H2O2 are involved in this process. Also, chelation of iron ions by means of desferrioxamine displayed a clear inhibitory action, suggesting the involvement of an iron-catalyzed Haber-Weiss-reaction leading to the formation of .OH radicals in the hepatotoxic response to ethanol. Our data suggest that during the metabolism of acetaldehyde primary reactive oxygen species (.O2-, H2O2) are produced which may interact to yield hydroxyl or .OH-like radicals, which possibly represent the hepatotoxic principle of ethanol.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
8755-0199
pubmed:author
pubmed:issnType
Print
pubmed:volume
3
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
19-26
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1987
pubmed:articleTitle
Alcohol-induced hepatotoxicity: a role for oxygen free radicals.
pubmed:affiliation
Institute of Toxicology, Medical University of Lübeck, W.-Germany.
pubmed:publicationType
Journal Article, In Vitro